Alison Feder
@alisonfeder.bsky.social
Rapid evolutionary dynamics in viruses, cancer and bacteria. Assistant professor at UW Genome Sciences and Freeman Hrabowski Scholar at HHMI. federlab.github.io
Amazing work, Ricky!!
December 17, 2025 at 9:22 PM
Amazing work, Ricky!!
Reposted by Alison Feder
If you are interested in this work and are looking for a postdoc position, please get in touch -- we are actively looking for someone to join our group at UCLA!
December 17, 2025 at 6:53 PM
If you are interested in this work and are looking for a postdoc position, please get in touch -- we are actively looking for someone to join our group at UCLA!
Amazing work, @rwolff.bsky.social and @nanditagarud.bsky.social!!!
December 17, 2025 at 9:14 PM
Amazing work, @rwolff.bsky.social and @nanditagarud.bsky.social!!!
Thanks so much, Asher! The project was much enriched by conversations I had at your sociovirology meeting in Puerto Rico!
December 15, 2025 at 5:07 PM
Thanks so much, Asher! The project was much enriched by conversations I had at your sociovirology meeting in Puerto Rico!
So much fun to work with Alex and Ben Kerr on this project, and to wade deeper into this exciting field of sociovirology. #socialviruses
We're also grateful for great suggestions from two anonymous reviewers during peer review.
www.nature.com/articles/s41...
We're also grateful for great suggestions from two anonymous reviewers during peer review.
www.nature.com/articles/s41...
Intracellular interactions shape antiviral resistance outcomes in poliovirus via eco-evolutionary feedback - Nature Ecology & Evolution
A model of intrahost poliovirus replication shows that, after several rounds of replication, pocapavir, a poliovirus capsid inhibitor, collapses viral density, preventing intracellular interactions th...
www.nature.com
December 10, 2025 at 9:07 PM
So much fun to work with Alex and Ben Kerr on this project, and to wade deeper into this exciting field of sociovirology. #socialviruses
We're also grateful for great suggestions from two anonymous reviewers during peer review.
www.nature.com/articles/s41...
We're also grateful for great suggestions from two anonymous reviewers during peer review.
www.nature.com/articles/s41...
Please check out the paper for our full results, and this nice press release put out by @uwnews.uw.edu!
newsroom.uw.edu/news-release...
newsroom.uw.edu/news-release...
Social lives of viruses affect antiviral effectiveness - UW Medicine | Newsroom
newsroom.uw.edu
December 10, 2025 at 9:07 PM
Please check out the paper for our full results, and this nice press release put out by @uwnews.uw.edu!
newsroom.uw.edu/news-release...
newsroom.uw.edu/news-release...
This parallels ongoing work in the treatment of cancers and bacteria showing that competitive inhibition and ecological interaction mediated by drug dosing can improve population control.
December 10, 2025 at 9:07 PM
This parallels ongoing work in the treatment of cancers and bacteria showing that competitive inhibition and ecological interaction mediated by drug dosing can improve population control.
Understanding this feedback could allow us to design more evolution-proof therapies by maintaining therapeutically useful social interactions over time.
@alexrob.bsky.social finds that neutralizing fewer viruses with weaker drugs can paradoxically lead to less resistance and lower viral loads.
@alexrob.bsky.social finds that neutralizing fewer viruses with weaker drugs can paradoxically lead to less resistance and lower viral loads.
December 10, 2025 at 9:07 PM
Understanding this feedback could allow us to design more evolution-proof therapies by maintaining therapeutically useful social interactions over time.
@alexrob.bsky.social finds that neutralizing fewer viruses with weaker drugs can paradoxically lead to less resistance and lower viral loads.
@alexrob.bsky.social finds that neutralizing fewer viruses with weaker drugs can paradoxically lead to less resistance and lower viral loads.
The point is much broader than poliovirus and pocapavir: if we're trying to design therapeutics that exploit social interactions between viruses, we need to account for the effects of therapeutic success in diminishing those interactions.
bsky.app/profile/alex...
bsky.app/profile/alex...
Big picture: the feedback loop between viral density leading to social interaction, which leads to realized phenotype, which alters fitness, leading to new viral densities, should be considered when designing optimal treatments.
December 10, 2025 at 9:07 PM
The point is much broader than poliovirus and pocapavir: if we're trying to design therapeutics that exploit social interactions between viruses, we need to account for the effects of therapeutic success in diminishing those interactions.
bsky.app/profile/alex...
bsky.app/profile/alex...
The answer? Sometimes! The key variable is the density of the viral population. When viruses coinfect often, interference is effective at arresting resistance evolution.
BUT, if the drug works well, it reduces viral density, ultimately allowing resistance to escape this interference.
BUT, if the drug works well, it reduces viral density, ultimately allowing resistance to escape this interference.
December 10, 2025 at 9:07 PM
The answer? Sometimes! The key variable is the density of the viral population. When viruses coinfect often, interference is effective at arresting resistance evolution.
BUT, if the drug works well, it reduces viral density, ultimately allowing resistance to escape this interference.
BUT, if the drug works well, it reduces viral density, ultimately allowing resistance to escape this interference.
In theory, this means that sus viruses should prevent resistance from spreading intra-host while it's rare.
Does it work? @alexrob.bsky.social built a poliovirus replication model to probe the impact of intra-cellular resource sharing, and validated it against experimental and clinical data.
Does it work? @alexrob.bsky.social built a poliovirus replication model to probe the impact of intra-cellular resource sharing, and validated it against experimental and clinical data.
December 10, 2025 at 9:07 PM
In theory, this means that sus viruses should prevent resistance from spreading intra-host while it's rare.
Does it work? @alexrob.bsky.social built a poliovirus replication model to probe the impact of intra-cellular resource sharing, and validated it against experimental and clinical data.
Does it work? @alexrob.bsky.social built a poliovirus replication model to probe the impact of intra-cellular resource sharing, and validated it against experimental and clinical data.
Pocapavir binds an oligomeric poliovirus capsid composed of 60 subunits.
Mutations can change this subunit's shape and prevent binding. However, if capsids contain both susceptible AND resistant subunits, drug can bind anyway.
As a result, sus viruses can sensitize res ones when they share a cell.
Mutations can change this subunit's shape and prevent binding. However, if capsids contain both susceptible AND resistant subunits, drug can bind anyway.
As a result, sus viruses can sensitize res ones when they share a cell.
December 10, 2025 at 9:07 PM
Pocapavir binds an oligomeric poliovirus capsid composed of 60 subunits.
Mutations can change this subunit's shape and prevent binding. However, if capsids contain both susceptible AND resistant subunits, drug can bind anyway.
As a result, sus viruses can sensitize res ones when they share a cell.
Mutations can change this subunit's shape and prevent binding. However, if capsids contain both susceptible AND resistant subunits, drug can bind anyway.
As a result, sus viruses can sensitize res ones when they share a cell.
Really enjoying reading your updates/highlights from the meeting! Thanks for posting!
October 29, 2025 at 9:53 PM
Really enjoying reading your updates/highlights from the meeting! Thanks for posting!